Experts at Indiana University School of Medicine have helped identify that a common protein found in neurodegenerative diseases forms amyloid filaments in an age-dependent manner without a connection to disease.

Many age-dependent neurodegenerative diseases, like Alzheimer's and Parkinson's, are characterized by amyloid abundance, or plaque. In a new paper published in Nature, researchers from the MRC Laboratory of Molecular Biology in Cambridge, England, United Kingdom and colleagues around the world, including several IU School of Medicine experts, used electron cryo-microscopy structure determination to discover that lysosomal type II transmembrane protein, TMEM106B, also forms amyloid filaments in human brains, but uniquely, it forms in an age-dependent manner and might not be connected to a type of disease.

"Until now, the presence of abundant intraneuronal amyloid filaments in human tissues has always been associated with disease," said Bernardino Ghetti, MD, a distinguished professor and professor of pathology and laboratory medicine at IU School of Medicine. "While TMEM106B has been associated with frontotemporal dementias and other diseases, the evidence for a causal relationship between TMEM106B aggregation and disease now remains unclear."

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